Melatonin
A hormone naturally produced by the pineal gland that regulates sleep-wake cycles, commonly supplemented for sleep disorders and jet lag.
Hormone precursors and adaptogens that support endocrine balance, thyroid function, and hormonal wellness.
5 itemsA hormone naturally produced by the pineal gland that regulates sleep-wake cycles, commonly supplemented for sleep disorders and jet lag.
Nicotinamide mononucleotide (NMN) is a direct precursor to NAD+ (nicotinamide adenine dinucleotide), a coenzyme found in every living cell that participates in over 500 enzymatic reactions. NAD+ is essential for mitochondrial energy production, DNA repair via PARP enzymes, and activation of sirtuins — a family of seven proteins often called "longevity regulators." NAD+ levels decline significantly with age — by roughly 50% between ages 40 and 60 in some tissues. This decline is implicated in mitochondrial dysfunction, impaired DNA repair, metabolic disorders, and the broader phenotype of aging. NMN supplementation aims to restore NAD+ levels by providing the immediate biosynthetic precursor. Animal studies have demonstrated remarkable results: improved insulin sensitivity, enhanced mitochondrial function, increased exercise endurance, and extended healthspan in aged mice. The first long-term human clinical trial (2022) showed that 250mg NMN daily for 12 weeks increased blood NAD+ levels and improved muscle function in older men. However, the field is still young, and optimal dosing, long-term safety, and definitive anti-aging effects in humans remain under investigation.
Thyroid disorders encompass underactive thyroid (hypothyroidism), overactive thyroid (hyperthyroidism/thyrotoxicosis), structural changes (goiter, nodules), and autoimmune conditions (Hashimoto’s thyroiditis, Graves’ disease). Western medicine defines and monitors thyroid status biochemically—principally using TSH, free T4, and when indicated, total/free T3 and thyroid antibodies (anti-TPO, anti-thyroglobulin, and TSH receptor antibodies [TRAb]). Imaging (ultrasound) and functional tests (radioactive iodine uptake [RAIU]) help characterize nodules and distinguish causes of thyrotoxicosis. Treatment decisions weigh severity, etiology, symptoms, pregnancy status, age, and comorbid risk (cardiovascular, bone). Hypothyroidism is most often autoimmune (Hashimoto’s) in iodine-sufficient regions. The gold standard treatment is levothyroxine (synthetic T4), titrated to normalize TSH and alleviate symptoms, with rechecks 6–8 weeks after dose changes and at steady state. Debate persists about adding liothyronine (T3) for persistent symptoms despite normalized TSH; current guidelines reserve combination therapy for carefully selected, monitored trials after ruling out other causes. Subclinical hypothyroidism (elevated TSH, normal FT4) management is individualized: treatment is favored when TSH ≥10 mIU/L, in pregnancy or infertility, with significant symptoms, goiter, positive TPO antibodies, or in younger patients planning conception; watchful waiting is often reasonable otherwise. Special attention to drug and nutrient interactions (iron, calcium, proton pump inhibitors, soy, high-fiber diets) and conditions that impair absorption (celiac disease, H. pylori, atrophic gastritis) is essential. Hyperthyroidism most commonly arises from Graves’ disease, toxic multinodular goiter, or a toxic adenoma. First-line options include antithyroid drugs (methimazole; propylthiouracil [PTU] in the first trimester of pregnancy or for thyroid storm), radioactive iodine ablation, and thyroid
Autoimmune diseases and thyroid disease intersect frequently because autoimmune thyroid diseases (AITD)—primarily Hashimoto’s thyroiditis and Graves’ disease—are among the most common organ‑specifi...
Hypothyroidism and depression frequently overlap clinically and biologically. Thyroid hormones influence brain development, neurotransmission, and energy metabolism; when thyroid levels are low (ov...